Skin and Photosensitivity

Summary:

This note discusses skin and photosensitivity, covering topics such as skin pigmentation, determining skin type, and oculocutaneous albinism. It also explores the photodermatoses and provides information on the history and clinical examination, as well as Xeroderma pigmentosum and variant xeroderma pigmentosum. The note goes on to discuss the porphyrias, medications causing photosensitivity, common photosensitive drugs, and associated features.

Other photosensitive disorders include phytophotodermatitis, polymorphous light eruption, solar urticaria, and chronic actinic dermatitis. The note concludes with a discussion on sun protection behaviour and sunscreens, as well as the relationship between vitamin D levels and sun protection.

Overall, this note provides a comprehensive overview of the skin and photosensitivity, covering a range of topics related to skin type, photodermatoses, medications, and common photosensitive disorders. It also offers useful insights into sun protection behaviours and the importance of maintaining vitamin D levels while staying protected from the sun

Excerpt:

Skin and Photosensitivity

Ultraviolet radiation
Ultraviolet radiation (UV) comprises 5% of all light penetrating the Earth’s atmosphere; 95%
is visible and infrared. Ultraviolet A (UVA) and ultraviolet B (UVB) wavelengths are known to play a
role in sun‐induced skin damage. The ozone layer filters out UVC. UV intensity is greatest near
the equator and at high altitudes. Other environmental factors, such as the season, weather, and
time of day, also influence intensity. UV is reflected by water (15%), snow (80%), and sand (25%).

Skin and Photosensitivity

Non‐ionising, visible, and infrared radiation

UVA photons have a longer wavelength (315–400 nm) and lower energy. They can
penetrate more deeply into the skin. UVA is present all year round and throughout the day at
constant levels. UVA can pass through glass and is important in skin tanning responses. UVA
can produce ‘reactive oxygen species’, which cause DNA, RNA, amino acid, protein, and
lipid damage.

UVB photons have a shorter wavelength (280–315 nm) and carry high energy. When UVB
hits the DNA, it causes mutations which can lead to keratinocyte apoptosis. When this occurs
in multiple keratinocytes at the same time, we call the ensuing inflammation ‘sunburn’. Some
UVB‐induced damage will be repaired, but ultimately the accumulated mutations in
cutaneous stem cells are the main cause of skin cancer.